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1

Ultrastructural picture of rat cerebellum in culture subjected to the action of antiglial immune serum

100%
Weinrauder H., Gajkowska B.
Bulletin of the Polish Academy of Sciences. Biological Sciences
|
1987
|
tom 35
|
nr 1-3
2

Effect of 3-aminobenzamide on Bcl-2, Bax and AIF localization in hippocampal neurons altered by ischemia reperfusion injury. The immunocytochemical study

100%
Strosznajder R., Gajkowska B.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 1
Poly(ADP-ribose) polymerase plays an important role in cell survival and death. Our previous histological and ultrastructural studies showed that PARP inhibitor 3-aminobenzamide (3-AB) protected neurons against death after ischemia. In this study we investigated the effect of 3-AB on the localization and expression of apoptosis inducing factor (AIF) and on two proteins from Bcl-2 family: Bcl-2 and Bax in hippocampal area CA1, on the 4th day after 3 min of forebrain ischemia in gerbils. Our results indicated that after ischemia AIF is preferentially translocated from the mitochondria to the cytoplasm and to the nucleus. Intravenous administration of 3-AB (30 mg/kg b.w.) prevents AIF translocation to the nucleus. AIF was mainly seen in the structurally unchanged mitochondria and Golgi complex. Moreover, after 3-AB administration overexpression of Bcl-2 protein was observed in mitochondrial membranes, rough endoplasmatic reticulum, Golgi complex, nuclear envelopes, and also in cytoplasm and in nucleus. These data suggest that inhibition of PARP activity may have a beneficial effect on hippocampal neurons through overexpression of Bcl-2 protein and suppression of AIF translocation to the nucleus.
3

Hypoxic damage of the cerebellum in 7-day-old rats. Ultrastructural and histochemical study

100%
Dambska M., Gajkowska B.
Acta Neurobiologiae Experimentalis
|
2002
|
tom 62
|
nr 1
4

Role of lipoxygenases and poly(ADP-ribose) polymerase in amyloid beta cytotoxicity

81%
Cieslik M., Strosznajder J. B., Gajkowska B., Strosznajder R. P.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
The roles of 12/15-lipoxygenase(s) (LOX), poly(ADP-ribose) polymerase (PARP-1) activity and mitochondrial apoptosis inducing factor (AIF) protein in the molecular processes evoked by amyloid β (Aβ) toxicity were investigated in PC12 cells that express either wild-type (APPwt) or double Swedish mutation (APPsw) forms of human Aβ precursor protein. Different levels of Aβ secretion characterize these cells. The results demonstrated a relationship between the Aβ levels and LOX protein expression and activity. High Aβ concentration in APPsw cells correlated with a significant increase in free radicals and LOX activation, which leads to translocation of p65/NF-κB into the nucleus. An increase in AIF expression in mitochondria was observed concurrently with inhibition of PARP-1 activity in the nuclear fraction of APPsw cells. AIF accumulation in mitochondria may be involved in adaptive/protective processes. However, inhibition of PARP-1 may be responsible for the disturbances in transcription and DNA repair as well as the degeneration of APP cells. Under conditions of increased nitrosative stress, evoked by the nitric oxide donor, sodium nitroprusside (SNP, 0.5 mM), 70-80 % of all cells types died after 24 h, significantly more in APPsw cells. There was no further significant change in mitochondrial AIF level and PARP-1 activity compared to corresponding nontreated with SNP cells. Only one exception was observed in PC12 control, where SNP significantly inhibits PARP-1 activity. Moreover, SNP significantly activated gene expression for 12/15-LOX in all types of investigated cells. Inhibitors of all LOX isoforms and specific inhibitor of 12-LOX enhanced the survival of cells that were subjected to SNP. We conclude that the LOX pathways may play a role in Aβ toxicity and in nitrosative-stress-induced cell death and that inhibition of these pathways offers novel protective strategies. Supported by MS&HE grant NN40113938 and MRC statutory theme No 7.
5

Autofagia w przebudowie gruczolu mlekowego bydla

81%
Gajewska M., Gajkowska B., Sobolewska A., Motyl T.
Medycyna Weterynaryjna
|
2007
|
tom 63
|
nr 11 Supl.
1412-1416
Autophagy is a process responsible for the degradation and recycling of cytoplasmic content by lysosomes. It is thought to facilitate cell survival during periods of nutrient starvation, but it can also be involved in other physiological processes including regulation of protein homeostasis, degrading intracellular bacteria, tumor suppression and regulation of programmed cell death. Our group was the first to report autophagy in bovine mammary epithelial cells, both in vitro, on BME-UV1 mammary epithelial cell line, and in vivo. The highest intensity of autophagy in bovine mammary glands is noted during dry periods, when the gland undergoes intensive involution and the deprivation of bioactive compounds (hormones, growth factors, cytokines) and nutrients occur. Our studies on the regulation of autophagy show that the conditions observed during bovine mammary gland involution, such as: 1) decrease in the release of lactogenic hormones and growth factors (prolactin, GH and IGF-I); 2) increase of apoptogenic factors (i.e. TGF-β₁) and their receptors, 3) increased synthesis of sex steroids (17-β estradiol, progesterone); and 4) the enhanced competition of intensively developing fetus and mother organism for nutritional and bioactive compounds, may create a state of temporary malnutrition of mammary epithelial cells that forces the cells to the induction of autophagy as a mechanism stabilizing intracellular supplies of energy and aminoacids, especially during the enhanced activity of apoptogenic factors.
6

Morfologiczne i molekularne wskazniki komorek macierzystych i progenitorowych w gruczole sutkowym

81%
Kolek O., Gajkowska B., Motyl T.
Medycyna Weterynaryjna
|
2008
|
tom 64
|
nr 02
136-141
The mammary gland is a dynamic organ that undergoes profound remodeling dependent on proliferation, differentiation, and apoptosis of mammary epithelial cells (MEC) during the cycle of the pregnancy, lactation, and involution. Long-lived populations of stem cells, which have a unique capacity for self-renewal, are responsible for these developmental changes. There is an increasing body of discoveries regarding human and mouse mammary gland stem cells, but the studies on bovine mammary gland stem cells are still very limited. According to morphological criteria bovine MEC are classified into two types: undifferentiated type I stem/progenitor cells assembling small light cells (SLC) and large light cells (LLC), and type II partially differentiated large dark cells (LDC) and terminally differentiated cells. To date there are no identified reliable molecular markers of stem/progenitor cells in bovine mammary glands. The main candidates are membrane transporting proteins of the Adenosine Binding Cassette (ABC) family, including Multi-drug-resistance protein 1 (Mdr1) and Breast cancer resistance protein 1 (Bcrp1). These proteins allow for the isolation of side populations (SP) of MEC assembling stem/progenitor cells by exclusion of dyes. Cytometric analysis of SP revealed from 0.2% to 5% of MEC in human and mouse mammary glands. The knowledge on the number and molecular properties of stem cells in bovine mammary glands would be very useful not only for enhancing milk production but also for explanation of the natural resistance against mammary cancer in this species.
7

Tratwy lipidowe w chorobie Alzheimera

81%
Kania E., Pajak B., Gajkowska B., Orzechowski A.
Postępy Biochemii
|
2012
|
tom 58
|
nr 2
8
Content available remote

Lipid rafts mediate epigallocatechin-3-gallate- and green tea extract-dependent viability of human colon adenocarcinoma COLO 205 cells; clusterin affects lipid rafts-associated signaling pathways

81%
Pajak B., Kania E., Gajkowska B., Orzechowski A.
Journal of Physiology and Pharmacology
|
2011
|
tom 62
|
nr 4
9

Mikrodomeny [rafty] lipidowe w blonach komorkowych: struktura, fizjologia i znaczenie w procesach patologicznych

81%
Wojewodzka U., Gajkowska B., Jurkiewicz J., Gniadecki R.
Postępy Biologii Komórki
|
2005
|
tom 32
|
nr 2
293-309
10

Ultrastructural studies on the nervous system in streptozotocine (STZ) - induced diabetes and experihental cerebral ischemia in the rat

81%
Piotrowski P., Gajkowska B., Olszewska H., Smialek M.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
11

Regulacja programowanej smierci komorki w przebudowie gruczolu mlekowego u bydla

81%
Motyl T., Zarzynska J., Gajewska M., Gajkowska B.
Folia Universitatis Agriculturae Stetinensis. Zootechnica
|
2006
|
tom 48
57-66
12
Content available remote

Apoptosis and autophagy induced by TGF-beta1 in bovine mammary epithelial BME-UV1 cells

81%
Gajewska M., Gajkowska B., Motyl T.
Journal of Physiology and Pharmacology. Supplement
|
2005
|
tom 56
|
nr 3
143-157
Mammary gland growth and involution is based on a dynamic equilibrium between proliferation and apoptosis of mammary gland epithelial cells (MEC). TGF-ß1 is an important antiproliferative and apoptogenic factor for mammary gland epithelial cells, acting in auto/paracrine matter and thus considered an important local regulator of mammary tissue involution. So far the studies on mammary gland involution concerned only apoptosis as a type I of MEC programmed cell death (PCD). Autophagy is known to be type II of PCD and this paper is the first, supporting evidence for the TGF-ß1-induced autophagy in bovine mammary epithelial cell line BME-UV1, as a distinct to apoptosis type of PCD. Laser scanning cytometry and confocal microscopy were used for analysis of MAP1 LC3 and Beclin1 expression - two proteins considered being the most reliable biochemical markers of autophagy. The significant increase of MAP1 LC3 and Beclin1 expression in cells treated with TGF-ß1 (2 ng/ml) was observed. Ultrastructural observation in electron microscopy revealed that autophagy is not only alternative, but also complementary to apoptosis type of cell death in TGF-ß1-treated bovine MEC. It was manifested by typical morphological features of apoptosis (cell shrinkage, margination and condensation of chromatin) and autophagy (autophagosomes, autophagic vacuoles) in the same cell.
13

Inflammation related apoptosis can be prevented by inhibition of nitric oxide synthesis

81%
Czapski G. A., Cakala M., Gajkowska B., Strosznajder J. B.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
14
Content available remote

Cycloheximide-mediated sensitization to TNF-alpha-induced apoptosis in human colorectal cancer cell line COLO 205: role of FLIP and metabolic inhibitors

81%
Pajak B., Gajkowska B., Orzechowski A.
Journal of Physiology and Pharmacology. Supplement
|
2005
|
tom 56
|
nr 3
101-118
Current efforts are focused on revealing the cellular factors that determine the “immune escape” of cancer cells. As an example in our study human colorectal cancer cell line COLO 205 was resistant to TNF-alpha - a death inducing ligand. Nonetheless, co-incubation TNF-alpha (10 ng/ml) with cycloheximide (5 µg/ml, CHX) caused time-dependent (6, 12, 24 hours) cell death even though, at that concentration cycloheximide did not exert cytotoxic effect unless 24 hour of treatment. After additional pretreatment it is concluded that CHX sensitizes cells to TNF-alpha-induced apoptosis. The aim of this study was to investigate the role and properties of cellular proteins that granted COLO 205 cells survival as well as to assess the effect of several metabolic inhibitors on cell viability at the above-mentioned time-points. PKCs inhibitor staurosporine (5 µM) did not influence, whereas cPKC activator PMA (100 µM) prevented TNF-alpha-induced apoptosis in the presence of CHX. Although EDTA (2 mM) and to a lesser degree EGTA (5 mM) were individually cytotoxic, they exerted protective effect at 6 and partially at 12 hour of combined TNF-alpha and CHX treatment. Ionophore A23187 (1 µM) protected cells against cell death at 12 and 24 but only partially at 6 hour of treatment. On the other hand, AD (10 ng/ml) acted synergistically with TNF-alpha and CHX at 6 and 12 hour. It appears that resistance of COLO 205 cells is determined on genomic level by a few reaction steps in which both Ca2+-dependent and antiapoptotic proteins are involved. Further studies revealed that CHX treatment reduces the level of FLIP but not other members of TNF-alpha-dependent death signalosome.
15
Content available remote

Cathepsins and BID are involved in the molecular switch between apoptosis and autophagy in breast cancer MCF-7 cells exposed to camptothecin

81%
Lamparska-Przybysz M., Gajkowska B., Motyl T.
Journal of Physiology and Pharmacology. Supplement
|
2005
|
tom 56
|
nr 3
159-179
The details of molecular switching points between apoptosis and autophagy in tumor cells have still not been fully elucidated. This study focused on the role of cathepsin B and its substrate, BID as molecular links between apoptosis and autophagy in human breast cancer MCF-7 cells exposed to camptothecin. Apoptosis occurred rapidly with a peak in 60 min after drug administration, whereas autophagy developed at a much slower rate with continuous progression during 24 h of cell exposure to the drug. CPT induced very rapid activation of cathepsin B. Inhibition of cathepsins by E64d prevented CPT-induced BAX and BID aggregation on mitochondria and reduced significantly reduced apoptotic cell number. The above effects were accompanied by an increase in autophagosome formation, measured by expression of MAP I LC3. BID knock down resulted in strong suppression of CPT-induced apoptosis and a shift of cell death towards autophagy, manifesting with an increase of Beclin 1 and MAP I LC3 cellular content.
16

Different composition of PSD after cerebral ischemia

81%
Zablocka B., Zalewska T., Gajkowska B., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
17
Content available remote

Position of STAT-1alpha in cycloheximide-dependent apoptosis triggered by TNF-alpha in human colorectal COLO 205 cancer cell line: role of polyphenolic compounds

81%
Pajak B., Gajkowska B., Orzechowski A.
Journal of Physiology and Pharmacology. Supplement
|
2005
|
tom 56
|
nr 3
119-141
“Immune escape” is a crucial instrument used by carcinoma cells to overcome numerous strategies of immune system to delete transformed cells. Cellular factors that make cancer cells immune to defence mechanisms are incompletely understood while some remain ambiguous. Up to date evidence points to some proteins and/or signaling molecules that might be a basis for unusual behavior of cancer cells. In particular STAT kinases are currently in the main focuse of attention since they were both shown to accelerate and/or to inhibit apoptosis. In our studies we observed that human colorectal COLO 205 cancer cells were resistant to TNF-alpha- or cycloheximide-induced cytotoxicity. However, when TNF-alpha (10 ng/ml) has been given along with cycloheximide (5 µg/ml, CHX) COLO 205 cells died extensively from apoptosis. Apparently, cycloheximide sensitized cells to TNF-alpha-induced programmed cell death. To investigate the role of STAT-1alpha in CHX-mediated TNF-alpha-induced COLO 205 cell death certain polyphenolic compounds were studied if they modulate STAT-1alpha phosphorylation status and STAT-1alpha-protein interaction at the level of TNF-alpha signalosome in the 6th, 12th, and 24th hour of experiment. Neither of phenolic compound, namely PI-3K inhibitor (LY294002, 20 µM) nor MEK inhibitor (PD98059, 50 µM), nor flavonol quercetin or kaempferol (10, 100 µM) in contrast to apigenin (20 µM) influenced COLO 205 cell viability during individual or combined treatment with TNF-alpha and CHX. We conclude, that some antiapoptotic proteins were involved but not STAT-1alpha kinase to resist TNF-alpha-dependent cell death promoting activity. Summing up, except apigenin, the above-mentioned polyphenolic componds were unable to modulate survival signal in COLO 205 cells initially believed to be suppressed by STAT-1alpha.
18

Molecular basis of parthenolide-dependent proapoptotic activity in cancer cells

81%
Pajak B., Gajkowska B., Orzechowski A.
Folia Histochemica et Cytobiologica
|
2008
|
tom 46
|
nr 2
129-135
19

Structure of cytomatrix and nuclear matrix revealed by embedment-free electron microscopy

81%
Gajkowska B., Cholewinski M., Gniadecki R.
Acta Neurobiologiae Experimentalis
|
2000
|
tom 60
|
nr 2
Embedment-free electron microscopy (EFEM) is a new method which allows the visualisation of cytoskeleton in whole-mounted cells. In this study we employed EFEM to investigate the structure of cellular scaffolds in glioma C6 cell line. The cells were extracted with Triton X-100 that dissolves phospholipids in the membranes and removes most of cytoplasmic soluble proteins. The DNA and nuclear histones were removed with DNase I and high-salt buffer, respectively. The remaining cellular frameworks were temporary embedded in diethylene glycol distearate (DGD), sectioned and observed in transmission and scanning electron microscope after the removal of DGD. The predominant structure was the extensive meshwork of 10-20 nm filaments in the cytoplasm (cytomatrix) and 15-30 nm filaments in the nucleus (nuclear matrix). The 5 nm filaments, presumably corresponding to the actin filaments, were present in the cytomatrix, but not in the nuclear matrix. Moreover, the ultrathin (3 nm) filaments, connecting other cytoskeletal components were detected. Those are possibly identical with the previously described plectin filaments. For the first time we report the occurrence of ultrathin filaments in the nuclear matrix. Thus, in a addition to the well known cytoskeletal components (microtubules, intermediate filaments, actin microfilaments) EFEM showed a new type of filaments (the ultrathin filaments) in the cytomatrix and nuclear matrix. Further immunocytochemical studies are needed to determine the biochemical identity of the filaments observed in EFEM.
20

Protein kinase C - like immunoreactivity in gerbil hippocampus after a transient cerebral ischemia

81%
Gajkowska B., Domanska-Janik K., Viron A.
Folia Histochemica et Cytobiologica
|
1994
|
tom 32
|
nr 2
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